title: Autophagy: a key pathway of TNF-induced inflammatory bone loss.
abstract: Autophagy describes the degradation of unnecessary or dysfunctional cellular components through the lysosomal machinery. Autophagy is essentially required to prevent accumulation of cellular damage and to ensure cellular homeostasis. Indeed, impaired autophagy has been implicated in a variety of different diseases. We examined the role of autophagy in inflammatory bone loss. We demonstrated that autophagy is activated by the pro-inflammatory cytokine tumor necrosis factor (TNF/TNFα) in osteoclasts of patients with rheumatoid arthritis (RA). Autophagy induces osteoclast differentiation and stimulates osteoclast-mediated bone resorption in vitro and in vivo, thereby highlighting autophagy as a novel mediator of TNF-induced bone resorption.
authors.affiliation: Department of Internal Medicine III and Institute for Clinical Immunology; University of Erlangen-Nuremberg; Erlangen, Germany.
authors.forename: Neng-Yu
authors.initials: NY
authors.lastname: Lin
authors.forename: Adrian
authors.initials: A
authors.lastname: Stefanica
authors.forename: Jörg H W
authors.initials: JH
authors.lastname: Distler
mesh_terms: D000818:Animals; D001169:Arthritis, Experimental / Q000276:immunology* / Q000473:pathology*; D001343:Autophagy / Q000276:immunology*; D007596:Joints / Q000473:pathology*; D014409:Tumor Necrosis Factor-alpha / Q000276:immunology*
chemical_list: D014409:Tumor Necrosis Factor-alpha
keywords: TNFÎ±; arthritis; autophagy; bone resorption; osteoclasts